Thin fiber muscle afferents (Aδ and C) are supplied by NaV 1.8 channels, whereas thick fiber afferents (spindles and tendon organs) are not. We determined the role played by NaV 1.8 channels on the thin fiber afferents evoking the reflex pressor response to femoral arterial injections of lactic acid (24mM; ~0.1mL) and capsaicin (0.1ug) in decerebrated Sprague Dawley rats with either patent or ligated femoral arteries. This was done both before and after femoral arterial injection of the A803467 (500µg, 1mg, and 2mg), a NaV 1.8 antagonist. We also recorded the responses of spindle afferents to succinylcholine (200µg) and stretch before and after injecting A803467. Rats were anesthetized with 2% isoflurane and 100% O2 until decerebration. In “freely perfused” rats (n=6), 1 mg of A803467 significantly reduced the pressor responses to lactic acid (16±5 to 4±4ΔmmHg) and capsaicin (47±7 to 26±8ΔmmHg). In “ligated” rats, 1 mg of A803467 significantly reduced the pressor response to lactic acid (32±13 to 3±3ΔmmHg, n=6), whereas 2 mg of A803467 was required to significantly reduce the pressor response to capsaicin (66±11 to 37±17ΔmmHg, n=4). Surprisingly, we found that A803467 (1mg) reduced the responses of 10 spindle afferents to succinylcholine (34±11 to 4±3 Δ imp/s p=0.04) and stretch (83±17 to 0.4±1 Δ imp/s; p<0.01). We conclude that A803467 reduces the chemoreflex response to lactic acid and capsaicin; however, it may be working on channels other than NaV 1.8 such as voltage-gated calcium channels.